In GBM, a biological consequence of altered subunit stoichiometry is easily possible: more β2 subunits linked to one KCa1.1 channel would mean complete channel inactivation, thus less driving force for Ca2+ signals, whereas more β3 subunits would lead to a rapid but incomplete channel inactivation (as can be seen in Fig. 4) and a prolonged Ca2+ influx. Here, KCNMA1 is linked to glioblastoma.